Antibiotic resistance is the ability of a microorganism to withstand the effects of an antibiotic.
Antibiotic resistance develops through mutation or plasmid exchange between bacteria of the same species. If a bacterium carries several resistance genes, it is called multiresistant or, informally, a superbug.

Causes

Antibiotic resistance is a consequence of evolution via natural selection. The antibiotic action is an environmental pressure; those bacteria which have a mutation allowing them to survive will live on to reproduce. They will then pass this trait to their offspring, which will be a fully resistant generation.

Several studies have demonstrated that patterns of antibiotic usage greatly affect the number of resistant organisms which develop. Overuse of broad-spectrum antibiotics, such as second and third generation cephalosporins, greatly hastens the development of methicillin resistance, even in organisms that have never been exposed to the selective pressure of methicillin per se. Other factors contributing towards resistance include incorrect diagnosis, unnecessary prescriptions, improper use of antibiotics by patients, and the use of antibiotics as livestock food additives for growth promotion.

Resistant pathogens

Staphylococcus aureus (colloquially known as "Staph aureus") is one of the major resistant pathogens. Found on the mucous membranes and the skin of around a third of the population, it is extremely adaptable to antibiotic pressure. It was the first bacterium in which penicillin resistance was found -- in 1947, just four years after the drug started being mass-produced. Methicillin was then the antibiotic of choice. MRSA (methicillin-resistant Staphylococcus aureus) was first detected in Britain in 1961 and is now "quite common" in hospitals. MRSA was responsible for 37% of fatal cases of blood poisoning in the UK in 1999, up from 4% in 1991. Half of all S. aureus infections in the US are resistant to penicillin, methicillin, tetracycline and erythromycin.

This left vancomycin as the only effective agent available at the time. However, VRSA (Vancomycin-resistant Staphylococcus aureus) was first identified in Japan in 1997 and has since been found in hospitals in England, France and the US. VRSA is also termed GISA (glycopeptide intermediate Staphylococcus aureus) or VISA (vancomycin intermediate Staphylococcus aureus), indicating resistance to all glycopeptide antibiotics.

A new class of antibiotics, oxazolidinones , became available in the 1990s, and the first commercially available oxazolidinone, linezolid, is comparable to vancomycin in effectiveness against MRSA. Linezolid-resistance in Staphylococcus aureus was reported in 2003.

Enterococcus faecium is another superbug found in hospitals: penicillin resistance was seen in 1983, vancomycin resistance (VRE) in 1987 and linezolid resistance (LRE) in the late 1990s.

Alternatives to antibiotics

Prevention

Wash hands properly to reduce the chance of getting sick and spreading infection. Wash fruits and vegetables thoroughly. Avoid raw eggs and undercooked meat, especially in ground form.
Do not demand antibiotics from your physician.
When given antibiotics, take them exactly as prescribed and complete the full course of treatment; do not hoard pills for later use or share leftover antibiotics.

Vaccines

Vaccines do not suffer the problem of resistance. This is because a vaccine enhances the body's natural defenses, while an antibiotic operates separately from the body's normal defenses. Nevertheless, new strains may evolve that escape immunity induced by vaccines.

While theoretically promising, anti-staphylococcal vaccines have shown limited efficacy, because of immunological variation between Staphylococcus species, and the limited duration of effectiveness of the antibodies produced. Development and testing of more effective vaccines is under way.

Phage therapy

Phage therapy is a more recent alternative that can cope with the problem of resistance.

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